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helping with wound healing. In addition, angiogenic processes and blood flow in the wound bed
decrease, acute wound metabolic activity slows down and eventually it stops, leading to mature scar
formation. Scar formation is the physiological endpoint of wound repair in mammals. When
excessive scarring occurs, there is an imbalance between biosynthesis and degradation, mediated by
apoptosis and ECM degradation, and this dysfunction leads to a persistent inflammatory phase, a
prolonged proliferation phase and reduced remodeling [32]. Hypertrophic scars contain excessive
microvessels, which are mostly occluded due to the over‐proliferation and functional regression of
endothelial cells, induced by myo‐fibroblastic hyperactivity and excessive collagen production.
Changes in ECM and the epithelium also appear to be involved in abnormal scarring; mechanical
stress stimulates skin mechanical–sensory nociceptors, which release neuropeptides involved in
vessel modification and fibroblast activation [5]
.
Figure 2. Stages of wound healing process: (a) physiological skin, (b) damaged skin, (c) skin
undergoing wound healing process and (d) healed skin. Histological image, hematoxylin–eosin, 10×,
bar: 20 μm, the red arrows highlight the named stages. Reproduction from: Dpt. Clinical–Surgical,
Diagnostic and Pediatric Sciences, University of Pavia.
3. Chronic Wound Care Treatment Approaches
3.1. Wound Care through TIME Principle
In the practice of wound care, the acronym Tissue (T), Infection (I), Moisture (M) and Epithelial
(E) (“TIME”) synthesizes all main factors that interfere negatively in the healing process. There is no
systematic way to assess acute injuries; therefore, TIME can be used as a practical guide for chronic
wound management [37]. In the acronym TIME are described some fundamental concepts that can
be grouped into four areas [38]: Tissue (T): evaluation and debridement of devitalized or non
self‐material in the wound bed (including necrotic tissue, adhering dressing material, biofilm or
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